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Chinese Medical Journal Mar 2015
Topics: Adult; Antitubercular Agents; Humans; Isoniazid; Male; Pulmonary Fibrosis
PubMed: 25698209
DOI: 10.4103/0366-6999.151695 -
Revue Des Maladies Respiratoires Mar 2022
Topics: Humans; Idiopathic Pulmonary Fibrosis; Pulmonary Medicine; Tomography, X-Ray Computed
PubMed: 35337709
DOI: 10.1016/j.rmr.2022.03.004 -
The Science of the Total Environment Jul 2022Airborne fine particulate matter (PM) is considered to be a risk factor for lung fibrosis, and therefore, it has attracted public attention due to its various...
Airborne fine particulate matter (PM) is considered to be a risk factor for lung fibrosis, and therefore, it has attracted public attention due to its various physicochemical features and its adverse effects on health. However, little remains to be known regarding the mechanism of PM-induced pulmonary fibrosis. The lung microbiota may be a potential factor involved in the adverse outcomes of pulmonary fibrosis. Meanwhile, miRNAs are thought to be key regulators that participate in the complex interplay between the host and the microbiota. Hence, to investigate the potential mechanisms of pulmonary fibrosis, and to explore the impact of PM-induced alterations in miRNAs and the lung microbiota and possible interaction patterns in mice models, we took advantage of 16S rDNA gene sequencing, miRNAs sequencing (miRNAs-Seq), and mining of public databases profiling. The results of 16S rDNA analysis showed that PM interfered with the microbial community composition, resulting in Proteobacteria becoming an additional dominant phylum. In addition, differentially expressed miRNAs were enriched in HIF-1 signaling, the IL-17 signaling, as well as Th17 cell differentiation pathways, which are closely related to microbial functional pathways. Significantly, a target miRNA, miR-149-5p, may be a key factor triggering the MAPK signal pathway related to pulmonary fibrosis and disturbing the homeostasis of lung bacterial flora. These results indicate that PM may lead to interaction between lung microbiota dysbiosis and an imbalance of miRNA levels to form a vicious cycle that promotes lung fibrogenesis. The current study provides new insights into the progression of pulmonary fibrosis.
Topics: Animals; DNA, Ribosomal; Lung; Mice; MicroRNAs; Microbiota; Particulate Matter; Pulmonary Fibrosis; Transcriptome
PubMed: 35378184
DOI: 10.1016/j.scitotenv.2022.154974 -
Respiratory Research Dec 2022Hypersensitivity pneumonitis (HP) is a type of interstitial lung disease (ILD) with a variable disease course and prognosis ranging from inflammatory and self-limiting...
BACKGROUND
Hypersensitivity pneumonitis (HP) is a type of interstitial lung disease (ILD) with a variable disease course and prognosis ranging from inflammatory and self-limiting to irreversible and progressive pulmonary fibrosis. Comorbidities are common in HP and may have an impact on prognosis. Due to the heterogeneity of HP presentation and progression, the identification of specific phenotypes in relationship to disease course and outcome is essential. The aim of this study was to identify clusters of comorbidities which could represent phenotypes in fibrotic HP and examine their impact on prognosis.
METHODS
Patients diagnosed with fibrotic HP at a tertiary referral center for ILD were included. Comorbidities were systematically registered and clusters of comorbidities were identified using cluster analyses. Disease progression and survival was estimated for each cluster.
RESULTS
The cohort comprised 211 patients with 53.6% males, mean age 63.0, baseline FVC 72.7%, DLCO 44.1%. Median follow-up time was 1.8 years (IQR 0.7-3.9). Three clusters with distinct comorbidity profiles and clinical characteristics were identified. One cluster dominated by elder male patients with predominantly cardiovascular diseases was associated with more respiratory hospitalizations and a worse prognosis. Differences in pulmonary function or exercise capacity trajectories between clusters were not observed.
CONCLUSIONS
Three clusters with distinct comorbidities were identified and could represent phenotypes in fibrotic HP not previously recognized. The worst prognosis was observed in a cluster dominated by elder males with cardiovascular diseases. Increased focus on prevention and treatment of comorbidities could potentially improve the prognosis of patients with fibrotic HP.
Topics: Male; Female; Humans; Cardiovascular Diseases; Lung Diseases, Interstitial; Alveolitis, Extrinsic Allergic; Pulmonary Fibrosis; Comorbidity
PubMed: 36539821
DOI: 10.1186/s12931-022-02291-4 -
Respiration; International Review of... 2017
Topics: Humans; Idiopathic Pulmonary Fibrosis; Pulmonary Fibrosis
PubMed: 28445891
DOI: 10.1159/000473884 -
Clinics in Chest Medicine Jun 2021Nonidiopathic pulmonary fibrosis (non-IPF) progressive fibrotic interstitial lung diseases (PF-ILDs) are a heterogeneous group of ILDs, often challenging to diagnose,... (Review)
Review
Nonidiopathic pulmonary fibrosis (non-IPF) progressive fibrotic interstitial lung diseases (PF-ILDs) are a heterogeneous group of ILDs, often challenging to diagnose, although an accurate diagnosis has significant implications for both treatment and prognosis. A subgroup of these patients experiences progressive deterioration in lung function, physical performance, and quality of life after conventional therapy. Risk factors for ILD progression include older age, lower baseline pulmonary function, and a usual interstitial pneumonia pattern. Management of non-IPF P-ILD is both pharmacologic and nonpharmacologic. Antifibrotic drugs, originally approved for IPF, have been considered in patients with other fibrotic ILD subtypes, with favorable results in clinical trials.
Topics: Humans; Lung Diseases, Interstitial; Pulmonary Fibrosis
PubMed: 34024407
DOI: 10.1016/j.ccm.2021.03.008 -
American Heart Journal Aug 2020Cardiovascular disease has an increased prevalence among patients with idiopathic pulmonary fibrosis (IPF). Cardiovascular disease and IPF share similar symptoms with... (Review)
Review
Cardiovascular disease has an increased prevalence among patients with idiopathic pulmonary fibrosis (IPF). Cardiovascular disease and IPF share similar symptoms with overlapping demographics and risk factors for disease development. Common cellular mediators leading to disease development and progression have been identified in both the cardiovascular and pulmonary organ systems. In this context, discovery of new therapeutic targets and medical therapies could be mutually beneficial across cardiopulmonary diseases. Here we present (1) a clinical review of IPF for the cardiovascular clinician and (2) common cellular mechanisms responsible for fibrosis in the heart and lungs and (3) highlight future research considerations and the potential role of novel therapeutic agents which may be mutually beneficial in cardiac and pulmonary fibrosis.
Topics: Algorithms; Cardiovascular Diseases; Humans; Idiopathic Pulmonary Fibrosis
PubMed: 32521292
DOI: 10.1016/j.ahj.2020.04.027 -
Zeitschrift Fur Rheumatologie Oct 2016Rheumatic diseases are frequently complicated by secondary pulmonary diseases, which often impair the quality of life and increase the mortality of patients. A correct... (Review)
Review
Rheumatic diseases are frequently complicated by secondary pulmonary diseases, which often impair the quality of life and increase the mortality of patients. A correct classification of such pulmonary complications is important to ensure appropriate treatment and optimal prognosis. The diagnostic and therapeutic challenge is to find the precise diagnosis and appropriate therapy among the multitude of potential causes for respiratory symptoms. It is important to maintain a cautious approach to invasive diagnostics, even though the differential diagnostics of infections or toxic lung disease might be crucial. The situation is further complicated by the frequent lack of evidence for therapies. Especially in the case of pulmonary fibrosis which is comparable to cancer in its complexity and high mortality, the diagnostics and therapy should be discussed in appropriate interdisciplinary boards.
Topics: Diagnosis, Differential; Evidence-Based Medicine; Germany; Humans; Pulmonary Fibrosis; Rheumatic Diseases; Risk Assessment; Treatment Outcome
PubMed: 27619368
DOI: 10.1007/s00393-016-0196-x -
Journal of Ethnopharmacology Jan 2024Pulmonary fibrosis (PF) is a chronic, progressive, and often fatal interstitial lung disease. Traditional Chinese medicine formulations and their active ingredients have...
ETHNOPHARMACOLOGICAL RELEVANCE
Pulmonary fibrosis (PF) is a chronic, progressive, and often fatal interstitial lung disease. Traditional Chinese medicine formulations and their active ingredients have shown potential in the treatment of PF. Panax notoginseng saponin (PNS) is extracted from the widely used traditional Chinese medicinal herb Panax notoginseng (Burkill) F. H. Chen, exhibiting therapeutic effects in pulmonary diseases treatment.
AIM OF THE STUDY
This study aimed to investigate the effects and elucidate possible potential mechanisms of PNS on bleomycin (BLM)-induced PF in rats.
MATERIALS AND METHODS
PF was induced in rats by intratracheal administration of bleomycin (BLM, 5 mg/kg). After disease model induction, the rats were treated with PNS (50, 100, or 200 mg/kg per day) or pirfenidone (PFD, 50 mg/kg per day) for 28 days. Lung function, histopathological changes, collagen deposition, and E- and N-cadherin levels in lung tissue were evaluated. The mechanism of action of PNS was investigated using tandem mass tag-based quantitative proteomics analysis. Immunohistochemistry, enzyme-linked immunosorbent assay (ELISA), and Western blot analysis were performed to verify the proteomic results.
RESULTS
PNS treatment improved lung function, ameliorated the BLM-induced increase in the lung coefficient, attenuated the degree of alveolar inflammation and fibrosis, and reduced the elevated collagen level in PF rats. PNS treatment also down-regulated the expression of N-cadherin while up-regulating the expression of E-cadherin. Proteomic and bioinformatic analyses revealed that the renin-angiotensin system (RAS) was closely related to the therapeutic effect of PNS. Immunohistochemistry, Western blot, and ELISA results indicated that PNS exerted its anti-fibrotic effect via regulation of the balance between the angiotensin-converting enzyme (ACE)-angiotensin (Ang)II-AngII receptor type 1 (AT1R) and ACE2-Ang(1-7)-MasR axes.
CONCLUSIONS
PNS ameliorates BLM-induced PF in rats by modulating the RAS homeostasis, and is a new potential therapeutic agent for PF.
Topics: Rats; Animals; Pulmonary Fibrosis; Renin-Angiotensin System; Panax notoginseng; Saponins; Proteomics; Fibrosis; Collagen; Bleomycin; Angiotensins
PubMed: 37532070
DOI: 10.1016/j.jep.2023.116979 -
European Respiratory Review : An... Dec 2021Acute manifestations of SARS-CoV-2 infection continue to impact the lives of many across the world. Post-acute sequelae of coronavirus disease 2019 (COVID-19) may affect... (Review)
Review
Acute manifestations of SARS-CoV-2 infection continue to impact the lives of many across the world. Post-acute sequelae of coronavirus disease 2019 (COVID-19) may affect 10-30% of survivors of COVID-19, and post-acute sequelae of COVID-19 (PASC)-pulmonary fibrosis is a long-term outcome associated with major morbidity. Data from prior coronavirus outbreaks (severe acute respiratory syndrome and Middle East respiratory syndrome) suggest that pulmonary fibrosis will contribute to long-term respiratory morbidity, suggesting that PASC-pulmonary fibrosis should be thoroughly screened for through pulmonary function testing and cross-sectional imaging. As data accumulates on the unique pathobiologic mechanisms underlying critical COVID-19, a focus on corollaries to the subacute and chronic profibrotic phenotype must be sought as well. Key aspects of acute COVID-19 pathobiology that may account for increased rates of pulmonary fibrosis include monocyte/macrophage-T-cell circuits, profibrotic RNA transcriptomics, protracted elevated levels of inflammatory cytokines, and duration of illness and ventilation. Mechanistic understanding of PASC-pulmonary fibrosis will be central in determining therapeutic options and will ultimately play a role in transplant considerations. Well-designed cohort studies and prospective clinical registries are needed. Clinicians, researchers and healthcare systems must actively address this complication of PASC to minimise disability, maximise quality of life and confront a post-COVID-19 global health crisis.
Topics: COVID-19; Humans; Pandemics; Prospective Studies; Pulmonary Fibrosis; Quality of Life; SARS-CoV-2
PubMed: 34911696
DOI: 10.1183/16000617.0194-2021